Evidence map›Paper›PMID 32729021›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2020

LncRNA PVT1 induces aggressive vasculogenic mimicry formation through activating the STAT3/Slug axis and epithelial-to-mesenchymal transition in gastric cancer.

Jing Zhao, Jing Wu, Yunyun Qin, Wenhong Zhang, Guangjian Huang, Lunxiu Qin

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  10. Vascular mimicry as a facilitator of melanoma brain metastasis.Cellular and molecular life sciences : CMLS · 2024
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  18. lncRNA PVT1: a novel oncogene in multiple cancers.Cellular & molecular biology letters · 2022
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Jing ZhaoDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai, 200040, People's Republic of China.ORCID http://orcid.org/0000-0003-2446-7732
Jing WuDepartment of Infectious Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, People's Republic of China.
Yunyun QinDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai, 200040, People's Republic of China.
Wenhong ZhangDepartment of Infectious Diseases, Huashan Hospital, Fudan University, Shanghai, 200040, People's Republic of China. zhangwenhong@fudan.edu.cn.
Guangjian HuangDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai, 200040, People's Republic of China. gjhuang@fudan.edu.cn.
Lunxiu QinDepartment of General Surgery, Huashan Hospital, Fudan University, Shanghai, 200040, People's Republic of China. qinlx@fudan.edu.cn.
Fudan University · CN

Funding

81201521 8120152181672378 81672378
6 · The paper itself

Abstract

purposeVasculogenic mimicry (VM), a vessel-like network formed by highly aggressive tumor cells, plays an important role in accelerating cancer progression. This special vascularization pattern is closely associated with a poor prognosis in various cancers. As yet, however, the regulatory mechanism of VM formation is largely unknown. In this study, we assess whether the long noncoding RNA PVT1 is involved in VM generation in gastric cancer.

methodsVM formation was determined by immunohistochemistry using PAS/CD31 double staining in gastric cancers and Matrigel tube formation in vitro. qRT-PCR and Western blotting were used to assess mRNA and protein expression. Interaction between PVT1 and STAT3 was determined using a RNA pull-down assay. Luciferase reporter and chromatin immunoprecipitation assays were performed to evaluate transcriptional activity of STAT3 on the Slug gene promoter.

resultsWe found that PVT1 can induce VM generation both in vitro and in vivo. Mechanistically, we found that PVT1 interacted with and activated STAT3 through a 850-1770 nt fragment. PVT1 facilitated STAT3 recruitment to the Slug promoter and transcriptionally enhanced Slug expression, thereby triggering epithelial-to-mesenchymal transition (EMT) and VM capillary formation. STAT3 inhibition effectively blocked PVT1-mediated VM. In primary gastric cancer samples, a positive correlation was found between PVT1 and Slug upregulation, and patients with a high PVT1 and Slug expression exhibited markedly shorter survival times.

conclusionOur results shed light on the role of PVT1 in gastric cancer cell-dependent VM formation. Our findings provide valuable clues for the design of new anti-angiogenic therapeutic strategies. The PVT1/STAT3 axis may serve as a potential target in gastric cancer treatment.

Indexed as

Molecular MimicryAnimalsBase SequenceCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMice, Inbred NODMice, SCIDModels, BiologicalNeoplasm InvasivenessPromoter Regions, GeneticRNA, Long NoncodingSnail Family Transcription FactorsSTAT3 Transcription FactorPVT1 long-non-coding RNA, humanRNA, Long NoncodingSNAI1 protein, humanSnail Family Transcription FactorsSTAT3 protein, humanSTAT3 Transcription FactorEpithelial-to-mesenchymal transitionGastric cancerPVT1SlugVasculogenic mimicry

Identifiers

PMID32729021
PMCPMC12990718
OpenAlexW3046193559

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.